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Prevalence of binary toxin positive Clostridium difficile in diarrhoeal humans in the absence of epidemic ribotype 027

Virulence of Clostridium difficile is primarily attributed to the large clostridial toxins A and B while the role of binary toxin (CDT) remains unclear. The prevalence of human strains of C. difficile possessing only CDT genes (A-B-CDT+) is generally low (< 5%), however, this genotype is commonly...

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Published in:PloS one 2017-11, Vol.12 (11), p.e0187658-e0187658
Main Authors: McGovern, Alan M, Androga, Grace O, Knight, Daniel R, Watson, Mark W, Elliott, Briony, Foster, Niki F, Chang, Barbara J, Riley, Thomas V
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description Virulence of Clostridium difficile is primarily attributed to the large clostridial toxins A and B while the role of binary toxin (CDT) remains unclear. The prevalence of human strains of C. difficile possessing only CDT genes (A-B-CDT+) is generally low (< 5%), however, this genotype is commonly found in neonatal livestock both in Australia and elsewhere. Zoonotic transmission of C. difficile has been suggested previously. Most human diagnostic tests will not detect A-B-CDT+ strains of C. difficile because they focus on detection of toxin A and/or B. We performed a prospective investigation into the prevalence and genetic characteristics of A-B-CDT+ C. difficile in symptomatic humans. All glutamate dehydrogenase or toxin B gene positive faecal specimens from symptomatic inpatients over 30 days (n = 43) were cultured by enrichment, and C. difficile PCR ribotypes (RTs) and toxin gene profiles determined. From 39 culture-positive specimens, 43 C. difficile isolates were recovered, including two A-B-CDT+ isolates. This corresponded to an A-B-CDT+ prevalence of 2/35 (5.7%) isolates possessing at least one toxin, 2/10 (20%) A-B- isolates, 2/3 CDT+ isolates and 1/28 (3.6%) presumed true CDI cases. No link to Australian livestock-associated C. difficile was found. Neither A-B-CDT+ isolate was the predominant A-B-CDT+ strain found in Australia, RT 033, nor did they belong to toxinotype XI. Previous reports infrequently describe A-B-CDT+ C. difficile in patients and strain collections but the prevalence of human A-B-CDT+ C. difficile is rarely investigated. This study highlights the occurrence of A-B-CDT+ strains of C. difficile in symptomatic patients, warranting further investigations of its role in human infection.
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The prevalence of human strains of C. difficile possessing only CDT genes (A-B-CDT+) is generally low (&lt; 5%), however, this genotype is commonly found in neonatal livestock both in Australia and elsewhere. Zoonotic transmission of C. difficile has been suggested previously. Most human diagnostic tests will not detect A-B-CDT+ strains of C. difficile because they focus on detection of toxin A and/or B. We performed a prospective investigation into the prevalence and genetic characteristics of A-B-CDT+ C. difficile in symptomatic humans. All glutamate dehydrogenase or toxin B gene positive faecal specimens from symptomatic inpatients over 30 days (n = 43) were cultured by enrichment, and C. difficile PCR ribotypes (RTs) and toxin gene profiles determined. From 39 culture-positive specimens, 43 C. difficile isolates were recovered, including two A-B-CDT+ isolates. 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The prevalence of human strains of C. difficile possessing only CDT genes (A-B-CDT+) is generally low (&lt; 5%), however, this genotype is commonly found in neonatal livestock both in Australia and elsewhere. Zoonotic transmission of C. difficile has been suggested previously. Most human diagnostic tests will not detect A-B-CDT+ strains of C. difficile because they focus on detection of toxin A and/or B. We performed a prospective investigation into the prevalence and genetic characteristics of A-B-CDT+ C. difficile in symptomatic humans. All glutamate dehydrogenase or toxin B gene positive faecal specimens from symptomatic inpatients over 30 days (n = 43) were cultured by enrichment, and C. difficile PCR ribotypes (RTs) and toxin gene profiles determined. From 39 culture-positive specimens, 43 C. difficile isolates were recovered, including two A-B-CDT+ isolates. This corresponded to an A-B-CDT+ prevalence of 2/35 (5.7%) isolates possessing at least one toxin, 2/10 (20%) A-B- isolates, 2/3 CDT+ isolates and 1/28 (3.6%) presumed true CDI cases. No link to Australian livestock-associated C. difficile was found. Neither A-B-CDT+ isolate was the predominant A-B-CDT+ strain found in Australia, RT 033, nor did they belong to toxinotype XI. Previous reports infrequently describe A-B-CDT+ C. difficile in patients and strain collections but the prevalence of human A-B-CDT+ C. difficile is rarely investigated. This study highlights the occurrence of A-B-CDT+ strains of C. difficile in symptomatic patients, warranting further investigations of its role in human infection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29117204</pmid><doi>10.1371/journal.pone.0187658</doi><tpages>e0187658</tpages><orcidid>https://orcid.org/0000-0002-1351-3740</orcidid><oa>free_for_read</oa></addata></record>
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source Open Access: PubMed Central; ProQuest - Publicly Available Content Database
subjects ADP Ribose Transferases - metabolism
Animals
Australia - epidemiology
Bacterial Proteins - metabolism
Bacterial toxins
Biology and Life Sciences
Causes of
Clostridium difficile
Clostridium difficile - classification
Clostridium difficile - genetics
Clostridium difficile - isolation & purification
Diagnosis
Diagnostic systems
Diarrhea
Diarrhea - epidemiology
Diarrhea - microbiology
Enzymes
Epidemics
Epidemiology
Genes
Genetic aspects
Genome, Bacterial
Genomes
Glutamate dehydrogenase
Health sciences
Hospitals
Humans
Infections
Laboratories
Livestock
Medicine
Medicine and Health Sciences
Microbiology
Neonates
Patients
People and Places
Physiological aspects
Polymerase chain reaction
Polymorphism, Single Nucleotide - genetics
Prevalence
Research and Analysis Methods
Ribotyping
Risk factors
Strains (organisms)
Toxin A
Toxin B
Toxins
Virulence
title Prevalence of binary toxin positive Clostridium difficile in diarrhoeal humans in the absence of epidemic ribotype 027
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